Simpaticotomía bilateral video asistida por hiperhidrosis: análisis de 102 pacientes / Bilateral video-assisted thoracic sympathicotomy for hiperhidrosis: analysis of 102 patients

Resumen La hiperhidrosis es un trastorno caracterizado por la producción excesiva de sudor por las glándulas sudoríparas ecrinas que influye negativamente en las actividades sociales, laborales y fundamentalmente en la calidad de vida. Se divide en primaria o secundaria. La primaria es una enfermedad benigna caracterizada por una excesiva sudoración con mayor frecuencia en palmas, plantas, axilas y cara. Su incidencia es del 1% de la población y su causa es desconocida. La mayoría de los tratamientos médicos no logran un buen control sintomático y frecuentemente son transitorios. La simpaticotomía torácica bilateral videoasistida se ha vuelto el tratamiento de elección en pacientes muy sintomáticos. En el período de 1998 a 2018 se realizaron 174 simpaticotomias bilaterales videoasistidas por hiperhidrosis primaria, de las cuales 102 cumplieron los criterios de inclusión. Se excluyeron a 72 pacientes. El 20.5% fueron hombres y el 79.5% mujeres con una edad media de 29.22 años. En cuanto a la localización fue palmoplantar axilar en un 50.9%, axilar en un 23.5%, palmoplantar en un 10.7%, palmar en un 7.8%, palmoaxilar 6.8% y facial 5.8%. Los pacientes con sudoración palmar presentaron 94.9% de mejoría, axilar 84.51%, plantar 46.25% y facial 84% respectivamente. El post operatorio arrojó una media de internación de 1.1 días. Como efecto no deseado, se presentó sudoración compensatoria en 53 casos y complicaciones postoperatorias en 18 casos. Concluimos que es una técnica segura, que resuelve de manera significativa la sudoración, mejorando la calidad de vida.

Abstract Hyperhidrosis is a disorder consisting of excessive sweating through the different body sweat glands, which produces a negative impact socially and in work-related activities in those that suffer this condition. There are primary and secondary forms. The primary form is a benign condition with excessive sweating mainly in palms, soles of feet, axillae and face. It affects a 1% of the population, and its cause is unknown. Most medical treatments are unsuccessful, and at best, transitory. In patients who are very troubled by the condition, videoassisted bilateral thoracic sympathicotomy has become the elective treatment. In the period ranging from 1998 to 2018, 174 procedures were undertaken for primary hyperhidrosis, of which 102 satisfied the inclusion criteria. 72 patients were excluded. A 20.5% were males, and 79.5% were females, with an average age of 29.22 years at surgery. As to localization of sweating, a 50.9% was palmar-plantar-axillary, 23.5% axillary, 10.7% palmarplantar, 7.8% palmar, 6.8% palmar-axillary, and a 5.8% facial. Those patients with palmar sweating showed a 94.9% improvement, those with axillary sweating a 88.51%, with plantar a 46.25% and those with facial sweating a 84% improvement. The average admission time was 1.1 days. As an undesired effect, compensatory sweating occurred in 53 cases and postoperative complications in 18 cases. We conclude this is a safe technique, that diminishes sweating significantly, improving patient's quality of life.

Objective evaluation of plantar hyperhidrosis after sympathectomy

OBJECTIVE: The aim of the present study was to prospectively, randomly, blindly, and objectively investigate how surgery affects plantar sudoresis in patients with palmar and plantar hyperhidrosis over a one-year period using a sudorometer (VapoMeter). METHODS: From February 2007 to May 2009, 40 consecutive patients with combined palmar hyperhidrosis and plantar hyperhidrosis underwent video-assisted thoracic sympathectomy at the T3 or T4 ganglion level (15 women and 25 men, with a mean age of 25 years). RESULTS: Immediately after the operation and during the one-year follow-up, all of the patients were free from palmar hyperhidrosis episodes. Compensatory hyperhidrosis of varying degrees was observed in 35 (87.5%) patients after one year. Only two (2.5%) patients suffered from severe compensatory hyperhidrosis. There was a large initial improvement in plantar hyperhidrosis in 46.25% of the cases, followed by a progressive regression of that improvement, such that only 30% continued to show this improvement after one year. The proportion of patients whose condition worsened increased progressively (from 21.25% to 47.50%), and the proportion of stable patients decreased (32.5% to 22.50%). This was not related to resection level; however, a lower intensity of plantar hyperhidrosis prior to sympathectomy correlated with worse evolution. CONCLUSION: Patients with palmar hyperhidrosis and plantar hyperhidrosis who underwent video-assisted thoracic sympathectomy to treat their palmar hyperhidrosis exhibited good initial improvement in plantar hyperhidrosis, which then decreased to lesser degrees of improvement over a one-year period following the surgery. For this reason, video-assisted thoracic sympathectomy should not be performed when only plantar hyperhidrosis is present.

Effect of Fluoxetine on Calcium or Potassium Channels in the Neuron of Rat Major Pelvic Ganglia / 대한비뇨기과학회지

PURPOSE: The major pelvic ganglia (MPG) provide the majority of the innervations to the lower urinary tract. The pelvic ganglia are unique autonomic ganglia that contain both sympathetic and parasympathetic neurons. It has been known that the low-threshold voltage-gated (T-type) Ca2 channels are only expressed only in the sympathetic neurons, whereas these channels are absent in parasympathetic neurons. In the present study, we examined the effect of fluoxetine, a world-wide used antidepressant, on the voltage-dependent Ca2 and K currents in the adrenergic neurons of the MPG. MATERIALS AND METHODS: The effect of fluoxetine on the voltage-dependent Ca2 and K currents in the adrenergic neurons of the MPG were examined using the whole-cell patch-clamp technique. RESULTS: Fluoxetine inhibited the voltage-activated Ca2 currents in the adrenergic neurons of the MPG. Both high-threshold (HVA) and low- threshold (LVA, T-type) Ca2 currents were inhibited by fluoxetine with an IC50 of 5.3 and 10.8microM, respectively. Fluoxetine also decreased the both the peak amplitude and the plateau of the outward K currents. The inhibition of the peak K currents by fluoxetine was concentration- dependent with an IC50 of 3.2microM. The inhibitions of the Ca2 and K currents were quickly reversible upon washout of the fluoxetine. CONCLUSIONS: These results provide evidence for the direct inhibition of the voltage dependant Ca2 and K currents by fluoxetine and these inhibitory effects could modify the synaptic transmission in adrenergic neurons of the MPG.

Characterization of Acetylcholine-induced Currents in Male Rat Pelvic Ganglion Neurons

The pelvic ganglia provide autonomic innervations to the various urogenital organs, such as the urinary bladder, prostate, and penis. It is well established that both sympathetic and parasympathetic synaptic transmissions in autonomic ganglia are mediated mainly by acetylcholine (ACh). Until now, however, the properties of ACh-induced currents and its receptors in pelvic ganglia have not clearly been elucidated. In the present study, biophysical characteristics and molecular nature of nicotinic acetylcholine receptors (nAChRs) were studied in sympathetic and parasympathetic major pelvic ganglion (MPG) neurons. MPG neurons isolated from male rat were enzymatically dissociated, and ionic currents were recorded by using the whole cell variant patch clamp technique. Total RNA from MPG neuron was prepared, and RT-PCR analysis was performed with specific primers for subunits of nAChRs. ACh dose-dependently elicited fast inward currents in both sympathetic and parasympathetic MPG neurons (EC50; 41.4microliterM and 64.0microliterM, respectively). ACh-induced currents showed a strong inward rectification with a reversal potential near 0 mV in current-voltage relationship. Pharmacologically, mecamylamine as a selective antagonist for alpha3beta4 nAChR potently inhibited the ACh-induced currents in sympathetic and parasympathetic neurons (IC50; 0.53micrometer and 0.22micrometer, respectively). Conversely, alpha- bungarotoxin, alpha-methyllycaconitine, and dihydro-beta-erythroidine, which are known as potent and sensitive blockers for alpha7 or alpha4beta2 nAChRs, below micromolar concentrations showed negligible effect. RT-PCR analysis revealed that alpha3 and beta4 subunits were predominantly expressed in MPG neurons. We suggest that MPG neurons have nAChRs containing alpha3 and beta4 subunits, and that their activation induces fast inward currents, possibly mediating the excitatory synaptic transmission in pelvic autonomic ganglia.

The Actions of Adenosine on Voltage-dependent K+ Currents in Neurons of Male Rat Major Pelvic Ganglia / 대한비뇨기과학회지

PURPOSE: The major pelvic ganglia (MPG) function as a relay center for autonomic pathways to the urogenital organs, such as the urinary bladder, vas deference, and penis. It is well known that adenosine acts as an important neuromodulator in various neuronal tissues. Several studies have suggested that some of these actions are coupled with potassium conductances. However, the exact mechanisms are unclear. Therefore, the roles of adenosine on the various potassium channels, in MPG neurons, were investigated. MATERIALS AND METHODS: Single neurons of the MPGs, located on the lateral surfaces of the prostate gland, from male rats were enzymatically dissociated. Ionic currents were recorded using the whole-cell variant patch-clamp technique. RESULTS: Two types of voltage-dependent outward potassium channels were isolated in the MPG neurons using whole-cell voltage protocols. One was the transient outward potassium current (type A-current, IA), the other was the delayed rectifier potassium current (IKDR). The IA and IKDR were recorded in both adrenergic and nonadrenergic neurons, which were distinguished by the existence of T-type calcium currents. Both the adrenergic and nonadrenergic neurons had the same kind of outward potassium currents. Application of adenosine (10(-4)M) increased the IA reversibly. N-cyclopentyladenosine (CPA, 10(-5)M), an A1 selective agonist, produced the same effect. However, the delayed rectifier components were not affected by the adenosine or CPA. The effects of adenosine and CPA on the IA were mostly prevented by pretreatment with DPCPX, an A1 selective antagonist. CONCLUSIONS: Adenosine increased the IA only, via the selective activation of A1 adenosine receptors. The augmentation of A-currents by adenosine may reduce neuronal firings, and then contribute to regulation of neuronal excitability in male rat MPG neurons.